Colorectal cancer in clinical practice : prevention, early by Rozen, P

By Rozen, P

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Extra resources for Colorectal cancer in clinical practice : prevention, early detection, and management

Sample text

Apoptosis fails to delete cell Clonal expansion, with altered cell relationships developing Benign neoplasia boring (paracrine) cells, bind to a receptor on the epithelial cell and modulate growth characteristics. Binding activates intracellular signaling pathways. g. mutation of the K-ras oncogene), the signaling pathway becomes continually and uncontrollably activated, and growth is no longer effectively regulated. Other similar disorders occur, such as with transforming growth factor b1 (TGF-b1) and its receptor.

Loss of chromosomal alleles is observed in larger adenomas. 17 4. 18 How do mutations and other genetic abnormalities arise? Mutations in the genome are either inherited or acquired. 1). Inherited mutations Inherited mutations may be direct and powerful, such as mutations of the APC gene responsible for FAP or of the DNA mismatch-repair genes (see below) responsible for hereditary non-polyposis colorectal cancer (HNPCC), or they may be indirect and less powerful, such as the genes that control metabolism of dietary procarcinogens.

With progression during tumorigenesis in the colon, chromosomal breaks and rearrangements become progressively frequent due to genomic instability, and so change the function of genes that maintain normal cell behavior. Single-base mispairs CTAGG_TTA GATCCGAT hMSH6 hMSH2 hMSH2 hMutScc hMSH6 hPMS2 hMSH2 hMLH1 DNA deletion Genes that maintain normal cellular homeostasis, especially proliferation and apoptosis, are known as tumor suppressor genes. Unlike oncogenes, which exert their influence by becoming active, these genes play a role because they are inactivated.

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